The exact cause of CPPD is unknown, although increased breakdown of adenosine triphosphate (ATP; the molecule used as energy currency in all living things), which results in increased pyrophosphate levels in joints, is thought to be one reason why crystals may develop.

Familial forms are rare. One genetic study found an association between CPPD and a region of chromosome 8q.

The gene ANKH is involved in crystal-related inflammatory reactions and inorganic phosphate transport.

CPPD affects people of all cultures and ethnic origins, and, in the United States, around 50% of the population over 85 years of age are affected. It may cause considerable pain, but it is never fatal. Women are at a slightly higher risk than men, with an estimated ratio of occurrence of 1.4:1.

A common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD).

Excessive calcium (due to hypomagnesemia) has a potential relationship with chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis.

Other causes of chondrocalcinosis include:

- Hypercalcaemia, especially when caused by hyperparathyroidism

- Arthritis

- Gout

- Wilson disease

- Hemochromatosis

- Ochronosis

- Hypothyroidism

- Hyperoxalemia

- Acromegaly

- osteoarthritis

Arthritis is the most common cause of disability in the USA. More than 20 million individuals with arthritis have severe limitations in function on a daily basis. Absenteeism and frequent visits to the physician are common in individuals who have arthritis. Arthritis can make it very difficult for individuals to be physically active and some become home bound.

It is estimated that the total cost of arthritis cases is close to $100 billion of which almost 50% is from lost earnings. Each year, arthritis results in nearly 1 million hospitalizations and close to 45 million outpatient visits to health care centers.

Decreased mobility, in combination with the above symptoms, can make it difficult for an individual to remain physically active, contributing to an increased risk of obesity, high cholesterol or vulnerability to heart disease. People with arthritis are also at increased risk of depression, which may be a response to numerous factors, including fear of worsening symptoms.

There are several diseases where joint pain is primary, and is considered the main feature. Generally when a person has "arthritis" it means that they have one of these diseases, which include:

- Osteoarthritis

- Rheumatoid arthritis

- Gout and pseudo-gout

- Septic arthritis

- Ankylosing spondylitis

- Juvenile idiopathic arthritis

- Still's disease

Joint pain can also be a symptom of other diseases. In this case, the arthritis is considered to be secondary to the main disease; these include:

- Psoriasis (Psoriatic arthritis)

- Reactive arthritis

- Ehlers-Danlos Syndrome

- Haemochromatosis

- Hepatitis

- Lyme disease

- Sjogren's disease

- Hashimoto's thyroiditis

- Celiac disease

- Non-celiac gluten sensitivity

- Inflammatory bowel disease (including Crohn's disease and ulcerative colitis)

- Henoch–Schönlein purpura

- Hyperimmunoglobulinemia D with recurrent fever

- Sarcoidosis

- Whipple's disease

- TNF receptor associated periodic syndrome

- Granulomatosis with polyangiitis (and many other vasculitis syndromes)

- Familial Mediterranean fever

- Systemic lupus erythematosus

An "undifferentiated arthritis" is an arthritis that does not fit into well-known clinical disease categories, possibly being an early stage of a definite rheumatic disease.

Prognosis varies with the type of amyloidosis. Prognosis for untreated AL amyloidosis is poor with median survival of one to two years. More specifically, AL amyloidosis can be classified as stage I, II or III based on cardiac biomarkers like troponin and BNP. Survival diminishes with increasing stage, with estimated survival of 26, 11 and 3.5 months at stages I, II and III, respectively.

Outcomes in a person with AA amyloidosis depend on the underlying disease and correlate with the concentration of serum amyloid A protein.

People with ATTR have better prognosis and may survive for over a decade.

Senile systemic amyloidosis was determined to be the primary cause of death for 70% of people over 110 who have been autopsied.

The three most common forms of amyloidosis are AL, AA, and ATTR amyloidoses. The median age at diagnosis is 64.

In the western hemisphere, AL is the most prevalent, comprising 90% of cases. In the United States it's estimated that there are 1,275 to 3,200 new cases of AL amyloidoses a year.

AA amyloidoses is the most common form in developing countries and can complicate longstanding infections with tuberculosis, osteomyleitis, and bronchiectesis. In the west, AA is more likely to occur from autoimmune inflammatory states. The most common causes of AA amyloidosis in the West are rheumatoid arthritis, inflammatory bowel disease, psoriasis, and familial Mediterranean fever.

People undergoing long term hemodialysis (14–15 years) can develop amyloidosis from accumulation of light chains of the HLA 1 complex which is normally filtered out by the kidneys.

Senile amyloidosis resulting from deposition of normal transthyretin, mainly in the heart, is found in 10–36% of people over 80.

Arthropathy may also include joint conditions caused by physical trauma to joints, but is traditionally used to describe the following conditions:

- "Reactive arthropathy" (M02-M03) is caused by an infection, but not a direct infection of the synovial space. (See also Reactive arthritis)

- "Enteropathic arthropathy" (M07) is caused by colitis and related conditions.

- "Crystal arthropathy" (also known as "crystal arthritis") (M10-M11) involves the deposition of crystals in the joint.

- In gout, the crystal is uric acid.

- In pseudogout/chondrocalcinosis/calcium pyrophosphate deposition disease, the crystal is calcium pyrophosphate.

- "Diabetic arthropathy" (M14.2, E10-E14) is caused by diabetes.

- "Neuropathic arthropathy" (M14.6) is associated with a loss of .

An arthropathy is a disease of a joint. Arthritis is a form of arthropathy that involves inflammation of one or more joints, while the term arthropathy may be used regardless of whether there is inflammation or not.

Spondylarthropathy is any form of arthropathy of the vertebral column.

Monoarthritis is inflammation ("arthritis") of one joint at a time. It is usually caused by trauma, infection, or crystalline arthritis.

In "gout", the acute inflammatory arthritis is caused by excess uric acid caused by either overproduction or under-excretion. Before the age of menopause, women have a lower incidence than males, but the rates are equal above this age. Gout can cause mono- or polyarthritis, but usually results in monoarthritis first.

Having more than one risk factor greatly increases risk of septic arthritis.

Risk of permanent impairment of the joint varies greatly. This usually depends on how quickly treatment is started after symptoms occur as longer lasting infections cause more destruction to the joint. The involved organism, age, preexisting arthritis, and other comorbidities can also increase this risk. Gonococcal arthritis generally does not cause long term impairment.

Mortality rates generally range from 10-20%. These rates increase depending on the offending organism, older age, and comorbidities such as rheumatoid arthritis

Chondrocalcinosis can be visualized on projectional radiography, CT scan, MRI, US, and nuclear medicine. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis and gout.

Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location i.e. around joints. The accumulations are outside the joint capsule. They are frequently seen in patients undergoing renal dialysis. It is also considered by some to have a hereditary predisposition. The name indicates calcinosis (calcium deposition) which resembles tumor (like a new growth). They are not true neoplasms - they don't have dividing cells. They are just deposition of inorganic calcium with serum exudate.

Children and adolescents (6 to 25 years) are the most commonly affected. The symptom that the accumulations cause is not pain but swelling around joints. They have propensity to enlarge progressively and ulcerate the overlying skin and extrude. They are most common around shoulders, hips and elbows. Laboratory evaluation reveal normal serum calcium levels and hyperphosphatemia. Rarely ALP (alkaline phosphatase - an enzyme active at sites of bone formation) may be elevated. Treatment is normalization of serum phosphate levels and resection of lesion. Surgical removal should be complete and if part of it is left, there is inevitable recurrence. Cutting through the excised calcium deposition reveals semifluid calcium suspension in albumin encapsulated by fibrous tissue.

Based on studies conducted in the United States, the prognosis for individuals with ALECT2 amyloidosis is guarded, particularly because they are elderly and their kidney disease is usually well-advanced at the time of presentation. End-stage renal disease develops in 1 out of 3 patients and has a median renal survival of 62 months. A suggested prognostic tool is to track creatinine levels in ALect2 patients. The attached Figure gives survival plotss for individuals with LECT2 renal amyloidosis and serum creatinine levels less than 2 mg/100 ml versus 2 mg/100 ml or greater than 2 mg/100 ml. The results show that afflicted individuals with lower creatinine levels have a ~four-fold higher survival rate.

Jaccoud arthropathy (JA), Jaccoud deformity or Jaccoud's arthopathy is a chronic non-erosive reversible joint disorder that may occur after repeated bouts of arthritis. It is caused by inflammation of the joint capsule and subsequent fibrotic retraction, causing ulnar deviation of the fingers, through metacarpophalangeal joint (MCP) subluxation, primarily of the ring and little-finger. Joints in the feet, knees and shoulders may also get affected. It is commonly associated with systemic lupus erythematosus (SLE), and occurs in roughly 5% of all cases.

When associated with rheumatic fever it is also called chronic post–RF arthropathy.

Originally thought to be associated only with rheumatic fever, it has since been shown to occur also in SLE, Sjögren syndrome, scleroderma, dermatomyositis, psoriatic arthritis, vasculitis, ankylosing spondylitis, mixed connective tissue disease, and pyrophosphate deposition disease. It is distinct from bone erosion which is commonly associated with rheumatic arthritis, and also distinct from mild deforming arthropathy which is associated with SLE. There have also been cases of non-rheumatic JA associated with Lyme disease, HIV-infection and a number of other conditions.

Treatment focuses toward alleviating pain and in maintaining functionality of the affected joints through use of nonsteroidal anti-inflammatory drugs, corticosteroids, antimalarial drugs and physiotherapy. Surgery is also a possibility, with osteotomy or stabilization with Kirschner intramedullary wire. Tendon relocation, however, has been shown to only work in 30% of cases. The condition is named after the French 19th century physician Sigismond Jaccoud.

Most individuals diagnosed with LECT2 amyloidosis in the United States (88%) are of Mexican descent and reside in Southwest region of the United States (New Mexico, Arizona, far Western Texas). Other groups with higher incidence rates of the disorder include First Nation Peoples in Canada, Punjabis, South Asians, Sudanese, Native Americans, and Egyptians. In Egyptians, for example, LECT2 is second most common cause of renal amyloidosis, accounting for nearly 31% of all cases.

ALECT2 amyloidosis is generally diagnosed in individuals between the ages 40 and 90, with a mean age of 67 years old. The disorder commonly presents with renal disease that in general is advanced or at an end stage. Associated signs and symptoms of their renal disease may include fatigue, dehydration, blood in urine, and/or other evidence for the presence of the nephrotic syndrome or renal failure. Further studies may find that these individuals have histological or other evidence of LECT2 amyloid deposition in the liver, lung, spleen, kidney, and/or adrenal glands but nonetheless they rarely show any symptoms or signs attributable to dysfunction in these organs. Unlike many other forms of systemic amyloidosis, LECT2 deposition has not been reported to be deposited in the myocardium or brain of affected individuals. Thus, LECT2 amyloidosis, while classified as a form of systemic amyloidosis, almost exclusively manifests clinically as renal amyloidosis. No familial link has been found in the disorder although there have been several cases described among siblings.

Causes of the swelling can include arthritis, injury to the ligaments of the knee, or an accident after which the body's natural reaction is to surround the knee with a protective fluid. There could also be an underlying disease or condition. The type of fluid that accumulates around the knee depends on the underlying disease, condition or type of traumatic injury that caused the excess fluid. The swelling can, in most cases, be easily cured.

Underlying diseases may include

- Knee osteoarthritis

- Rheumatoid arthritis

- Infection

- Gout

- Pseudogout

- Prepatellar bursitis (kneecap bursitis)

- Cysts

- Tumours

- Repetitive strain injury

Having osteoarthritis or engaging in high-risk sports that involve rapid cut-and-run movements of the knee — football or tennis, for example — means an individual is more likely to develop water on the knee.

In overweight or obese individuals the body places more weight on the knee joint. This causes more wear in the joint. Over time, the body may produce excess joint fluid.

There is no clear obvious cause for scleroderma and systemic sclerosis. Genetic predisposition appears to be limited: genetic concordance is small; still, there is often a familial predisposition for autoimmune disease. Polymorphisms in "COL1A2" and "TGF-β1" may influence severity and development of the disease. There is limited evidence implicating cytomegalovirus (CMV) as the original epitope of the immune reaction, as well as parvovirus B19. Organic solvents and other chemical agents have been linked with scleroderma.

One of the suspected mechanisms behind the autoimmune phenomenon is the existence of microchimerism, i.e. fetal cells circulating in maternal blood, triggering an immune reaction to what is perceived as foreign material.

A distinct form of scleroderma and systemic sclerosis may develop in patients with chronic renal failure. This form, nephrogenic fibrosing dermopathy or nephrogenic systemic fibrosis, has been linked to exposure to gadolinium-containing radiocontrast.

Bleomycin (a chemotherapeutic agent) and possibly taxane chemotherapy may cause scleroderma, and occupational exposure to solvents has been linked with an increased risk of systemic sclerosis.

Paget's disease may be caused by a slow virus infection (i.e., paramyxoviridae) present for many years before symptoms appear. Associated viral infections include respiratory syncytial virus, canine distemper virus, and the measles virus. However, recent evidence has cast some doubt upon the measles association. Laboratory contamination may have played a role in past studies linking paramyxovirus (e.g. measles) to Paget's disease.

The median time to progression to end stage renal disease is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have end stage renal disease.

Pagets disease of bone is the second most common metabolic bone disorder, after osteoporosis. The overall prevalence and severity of Paget's disease are decreasing; the cause for these changes is unclear. Paget's disease is rare in people less than 55 years of age, and the prevalence increases with age. Evidence from studies of autopsy results have demonstrated Paget's disease in about 3 percent of people older than 40 years of age. Paget's disease is more common in males than females. Rates of Paget's disease are about 50 percent higher in men than in women.

About 15 percent of people with Paget's disease also have a family member with the disease. In cases where the disease is familial, it is inherited in an autosomal dominant fashion, although not all people that inherit the affected version of the genes will express the disease (incomplete penetrance).

The incidence of Paget's disease varies considerably with geographic location. Paget's predominantly affects people of European descent, whereas people of African, Asian, or Indian descent are less commonly affected. Paget's disease is less common in Switzerland and Scandinavia than in the rest of Western Europe. Paget's disease is uncommon in the native populations of North and South America, Africa, Asia, and the Middle East. When an individual from these regions does develop Paget's disease, there is typically some European ancestry present.

The 5-year survival rate for scleroderma is about 85%, whereas the 10-year survival rate is less than 70%. This varies according to the subtype; for instance, persons with limited skin disease have a 10-year survival rate of 71%, whereas the outlook for patients with systemic scleroderma has generally improved over the years. Ten-year survival rates rose from 54% in 1972 to 66% in 2001 The major causes of death in persons with scleroderma are: pulmonary hypertension, pulmonary fibrosis and scleroderma renal crisis. People with scleroderma are also at a heightened risk for contracting cancers (especially liver, lung, haematologic and bladder cancers) and, perhaps, cardiovascular disease.

Scleroderma in pregnancy is a complex situation; it increases the risk to both mother and child. Overall scleroderma is associated with reduced fetal weight for gestational age. The treatment for scleroderma often includes known teratogens such as cyclophosphamide, methotrexate, mycophenolate, etc. and hence careful avoidance of such drugs during pregnancy is advised. In these cases hydroxychloroquine and low-dose corticosteroids might be used for disease control.